The invention generally relates to the treatment of congestive heart failure (CHF). In particular, the invention relates to a method and apparatus to treat patients with congestive heart failure by normalization of kidney perfusion to restore to the patient the benefits of normal kidney functioning.
A. Congestive Heart Failure (CHF)
Congestive heart failure (CHF) is a serious condition affecting an estimated 5 million Americans. Increasing prevalence, hospitalizations, and deaths have made CHF a major chronic health condition in the United States. There are an estimated 400,000 new cases of CHF each year. These cases are often first diagnosed as the end stage of cardiac disease. The average mortality rate of CHF is 10 percent after the 1st year and 50 percent after 5 years. Thus, half of the patients diagnosed with CHF will die within 5 years of their diagnosis.
The magnitude of the problem is expected to get much worse as more cardiac patients are able to survive and live longer. As patients live longer, the potential for developing CHF increases. In addition, because the incidence of heart failure rises substantially beyond age 65, the prevalence of this condition is likely to increase as the population ages.
The high prevalence of heart failure and the resulting high cost of caring for these patients places a significant economic burden on society. The American Heart Association statistics report that, including medications, an estimated $22.5 billion will be spent for the care of CHF patients in hospitals, physicians offices, home care, and nursing homes including medications in the year 2000. In light of the high costs and poor prognosis of CHF, there is a pressing need to prevent this condition and provide better clinical management to reduce morbidity and mortality.
Congestive heart failure (CHF) is a diseased condition in which the heart fails to function efficiently as a pump to provide sufficient blood flow and/or pressure to fulfill the normal circulatory needs of a patient. CHF is the primary reason for tens of thousands of deaths each year and is a contributing factor in an additional 200,000 more deaths. CHF results in sudden shortness of breath, fainting and irregular heart beats that require frequent emergency room treatments (acute CHF), and in its chronic form leads to repeated hospital stays, deteriorating quality of life and significant costs to the health care system. Congestive heart failure is characterized by: (1) signs and symptoms of intravascular and interstitial volume overload, including shortness of breath, fluid in the lungs, and edema, and (2) manifestations of inadequate tissue perfusion, such as fatigue or poor exercise tolerance. These signs and symptoms result when the heart is unable to generate a cardiac output sufficient to meet the body""s demands.
A healthy heart pumps blood by increasing the kinetic energy (pressure and/or velocity) of the blood flowing through a person""s circulatory system. The energy imparted by a heart to the blood flow is normally sufficient to cause the blood to circulate through the lungs, kidney and other organs of the body. A failing heart is generally unable to maintain normal blood pressure within the circulatory system of a person. The body responds to a failing heart by diverting much of the available blood flow to the brain and heart and reducing the blood flow to other body organs, including the kidneys. Thus, the body acts to save the brain (which cannot survive more than a few minutes of inadequate blood flow).
The heart ejects oxygen-enriched blood into the aorta, which is a huge blood vessel, from which branches all other arteries that lead to the different organs of the body. These organs use the oxygen from the arterial blood. Used blood deprived of oxygen and containing the metabolic byproduct carbon dioxide is collected from the organs via individual veins and is returned to the lungs via the pulmonary vein. Accordingly, the heart pumps the blood into the aorta and forces the blood to circulate through the arteries, organs, veins and lungs.
Arteries by expanding or contracting regulate the blood supply flowing to individual tissues and organs. Arterial walls are made of thin layers of muscle fibers that expand and contract. The expansion and contraction of the arteries controls the flow of blood through a patient""s circulatory system in a manner similar to the way valves control the flow of water through the water pipes in a home. The arterial walls contract or relax responding to different stimuli decreasing or increasing the inner cross section of the vessel. The contraction of the arteries is called vasoconstriction and the relaxation is called vasodilation. In this manner, depending on the oxygen needs of an organ or tissue, arterial blood flow is controlled and the supply of oxygen rich blood is regulated. Only as much arterial blood as needed is supplied to organs depending on the functions they are performing at the time.
When the demand for oxygen delivery from the blood exceeds the available blood supply for a particular organ, the organ becomes ischemic (which is a condition in which minimized blood flow can lead to oxygen starvation of an organ). If allowed to persist, ischemia leads to severe tissue damage. The complex network of neurohormonal messengers indicates to the brain that the blood supplied by the heart and the blood vessels is not sufficient to support the current metabolic needs of that organ. The body reacts to ischemic by supplying more blood to the organ(s) needing more oxygen in order of priority. For example, the legs of a human runner get more blood during exercise because the leg muscles are working hard and need extra oxygen. Similarly, the runner""s gut receives an increase of blood flow when food is digested. If the runner tries to eat and run at the same time, he may get cramps in the legs or stomach pain because of ischemia. The brain reacts by altering the autonomic nervous system activity and neurohormonal secretions to attempt to divert additional blood flow from other organs to augment the blood supply to the ischemic organs to meet their metabolic demands. Accordingly, in a healthy patient, the circulatory system is adjusted by the brain so that all organs receive adequate blood supply. However, the body cannot supply adequate blood flow to all organs when the heart begins to fail during CHF. The ultimate priority for the body is always to maintain sufficient blood pressure in the aorta at any cost to protect the brain.
Heart failure is not simply a disease of the heart, but rather is a complex disease process that involves interaction of many of the body""s systems. It is believed that the body reaction to a signal of low blood pressure is based on the body""s interpretation that it has suffered a severe injury that caused massive bleeding. In this situation, the body attempts to reduce the probability of death from low blood pressure by diverting blood flow away from the organs that can temporarily tolerate ischemia (e.g., the body extremities, liver and kidneys) to the vital organs (brain and heart) that cannot tolerate even momentary ischemia (such as the brain and heart). In the situation of bleeding, if the bleeding stops in a brief amount of time, the blood pressure will rise in the circulatory system. As blood pressure rises, the body will restore normal blood flow through the entire circulatory system and to all body organs. It appears that evolution has adapted the human body to react to severely reduced blood pressure by temporarily reducing blood flow to less vital organs such as limbs, gut or kidney. This reaction assumes that normal blood pressure will be quickly restored or the person will die from their injuries.
This same originally beneficial evolutionary reaction to reduced blood pressure appears to be deleterious in the setting of congestive heart failure. Congestive heart failure is not relieved by reducing blood flow to body organs and body exterminates. In fact, CHF is not a temporary reduction in blood pressure, but instead is characterized by reduced blood pressure for weeks, months and years of a patient""s life. Moreover, CHF is a relatively recent condition to which the body has not adapted by evolution. Accordingly, it is believed that the body""s response in CHF causes many body organs, such as the kidney, to receive inadequate blood flow for too long a period of time. As these organs shut down due to inadequate blood flow, they are no longer able to perform their normal physiological functions.
Congestive heart failure can be either acute and/or chronic. Acute CHF occurs suddenly and often requires emergency treatment. Chronic CHF is a slowly deteriorating condition that continuously worsens and often requires repeated treatments in the hospital.
In both conditions the failing heart is not be able to generate sufficient blood pressure to properly perfuse the kidneys, e.g., provide sufficient blood pressure to force blood through the kidneys and filter the blood. In a patient suffering form chronic heart failure, the blood pressure tends to progressively decrease as the heart progressively fails over weeks, months and/or years. With the decrease in blood pressure there is a concomitant decrease in organ perfusion. Accordingly, chronic heart failure can lead to chronic impaired renal perfusion. Treatments for chronic CHF must be able administered repeatedly to a patient, preferably in a clinic or other no intensive critical-care unit (ICU) of a hospital without causing injury to the patient or reduce the physician""s capacity to perform repeated therapy.
Chronic heart failure patients are frequently admitted to hospital with an abrupt worsening of their condition that requires intensive care (termed, acute heart failure). During these periods of acute hypotension (or low blood pressure) their kidneys are particularly at risk from hypotension and can be severely injured. In some cases the blood pressure of these patients can be normal but at the expense of the total shutdown of the blood flow to the kidneys. Kidneys of these patient are as much (or more) in jeopardy as the ones of the patients with low blood pressure. Because of its emergency nature, treatments of acute CHF must be fast-acting and thus may be extremely invasive and may require the patient to be admitted to an ICU. Thus, the apparatus for treating acute CHF are often fast acting and quickly administered, which may result, for example, in a rapid surgical insertion of a large catheter into an artery of the patient. The apparatus suitable for treating acute CHF may not be appropriate for repeated courses of treatments required for patients with chronic CHF. Because repeated treatments are required, the apparatus for treating chronic CHF should be adapted to be applied to the patient without the need for surgery or invasively entering the circulatory system under fluoroscopy that requires catheterization lab equipment. Accordingly, a different apparatus may be needed for treating chronic and acute CHF, even though the same method of treatment, e.g., perfusing a kidney, is performed by both apparatus.
B. Relationship Of Kidney Failure To CHF
The kidneys are a pair of organs that lie in the back of the abdomen on each side of the vertebral column. They play an important regulatory role in maintaining the homeostatic balance of the body. The kidneys function like a complex chemical plant. The kidneys eliminate foreign chemicals from the body, regulate inorganic substances and the extracellular fluid, and function as endocrine glands, secreting hormonal substances like renin and erythropoietin.
The main functions of the kidney are to maintain the water balance of the body and control metabolic homeostasis. The kidneys regulate the amount of fluid in the body by making the urine more or less concentrated, thus either reabsorbing or excreting more fluid, respectively. A large amount of blood (approximately 1,500 liters per day) passes through the kidneys. Of that, about 98% of the filtered fluid is reabsorbed. In addition, the kidneys extract undesirable chemicals and concentrate them in urine, while allowing the reabsorbtion of other chemicals. These processes of filtration, reabsorbtion and fluid regulation take place in the renal nephron. Within the nephron the smallest circulatory vessels, capillaries and arterioles, form a glomerulus. This glomerulous is intimatelly associated with the renal tubules to filter wastes from the blood, remove excess water from the body and produce concentrated urine. The glomerular filtration rate (GFR) is a clinical indicator universally accepted as a measure of the ability of the kidney to remove fluid and solutes. In other words, GFR is the summary of the physiologic functions of the kidneys.
A kidney, like any other organ, needs oxygen from the blood stream to function. The kidneys remove only a small amount of amount of the deleterious metabolic products from each portion of the blood to which they exposed. Thus, the blood is repeatedly circulated through the kidney many times during each day to remove the required amount of these substances. Under normal conditions in a healthy person, the kidney must receive approximately 10% of the cardiac output (total body blood flow) or 0.5 liters per minute which, over the course of a day, amounts to 720 liters per day of blood passing through each kidney. Significantly, more fluid is filtered through the kidneys than is excreted as urine. Most of the filtered fluid must be reabsorbed into the circulatory system to maintain the fluid balance of the body. In case of CHF, some normal and important physi-ological functions become detrimental to the patient""s health. This process is sometimes called maladaption.
Without properly functioning kidneys, a patient will suffer water retention, reduced urine flow and an accumulation of wastes toxins in the blood and body. These conditions resulting from reduced renal function or renal failure (kidney failure) are believed to increase the workload of the heart. In a CHF patient, renal failure will cause the heart to further deteriorate as the water build-up and blood toxins accumulate due to the poorly functioning kidneys and in turn, cause the heart further harm.
FIG. 6 is a chart that illustrates the cycle of CHF as it relates to renal failure of the kidneys. In step 100 of CHF, for any of the known cause of heart dysfunction, the heart will progressively fail and blood flow and pressure will drop in the patient""s circulatory system. In the acute heart failure, the short-term compensations serve to maintain perfusion to critical organs, notably the brain and the heart that cannot survive prolonged reduction in blood flow. In chronic heart failure, these same responses that initially aided survival in acute heart failure can become deleterious.
A combination of complex mechanisms contribute to the deleterious fluid overload in CHF. As the heart fails and blood pressure drops, the kidneys cannot function owing to insufficient blood pressure for perfusion and become impaired in step 102. This impairment in renal function ultimately leads to a decrease in urine output in step 103. Without sufficient urine output, the body retains fluids and the resulting fluid overload causes peripheral edema (swelling of the legs), shortness of breath (from fluid in the lungs), and fluid in the abdomen, among others undesirable conditions in the patient.
In addition, the fall in cardiac output leads to reduced renal blood low, increased neurohormonal stimulus, and release of the hormone renin from the juxtaglomerular apparatus of the kidney, in step 104. This results in avid retention of sodium and thus volume expansion, 106. Increased rennin results in the formation of angiotensin, a potent vasoconstrictor, 105.
Heart failure and it""s the resulting reduction in blood pressure reduces the blood flow and perfusion pressure through organs in the body 108, other than the kidneys. As these other organs suffer reduced blood pressure, these organs may become hypoxic causing the development of a metabolic acidosis 109 which reduces the effectiveness of pharmacological therapy as well as increases the risk of sudden death
This spiral of deterioration that physicians observe in heart failure patients is believed to be mediated in large part, by activation of a subtle interaction between heart function and kidney function, known as the renin-angiotensin system. Disturbances in the heart""s pumping function results in decreased cardiac output and diminished blood flow 100. The kidneys respond to the diminished blood flow as though the total blood volume was decreased, when in fact the measured volume is normal or even increased 102. This leads to fluid retention by the kidneys 106 and formation of edema causing fluid overload and increased stress on the heart 107.
Systemically, CHF is associated with an abnormally elevated peripheral vascular resistance and is dominated by alterations of the circulation resulting from an intense disturbance of sympathetic nervous system function. Increased activity of the sympathetic nervous system promotes a downward vicious cycle of increased arterial vasoconstriction (increased resistance of vessels to blood flow) followed by a further reduction of cardiac output, causing even more diminished blood flow to the vital organs.
In CHF via the previously explained mechanism of vasoconstriction, the heart and circulatory system dramatically reduce blood flow to kidneys. In addition, during CHF the kidneys receive a command from higher neural centers via neural pathways and hormonal messengers to retain fluid and sodium in the body. In response to stress on the heart, the neural centers command the kidneys to reduce their filtering functions. While in the short term these commands can be beneficial, if these commands continue over hours and days they can jeopardize the persons life or make the person dependent on artificial kidney for life by causing the kidneys to cease functioning.
When the kidneys do not fully filter the blood, a huge amount of fluid is retained in the body resulting in bloating (fluid in tissues), and increases the workload of the heart. Fluid can penetrate into the lungs and the patient becomes short of breath. This odd and self-destructive phenomenon is most likely explained by the effects of normal compensatory mechanisms of the body that improperly perceive the chronically low blood pressure of CHF as a sign of temporary disturbance such as bleeding.
In an acute situation, the organism tries to protect its most vital organs, the brain and the heart, from the hazards of oxygen deprivation. Commands are issued via neural and hormonal pathways/messengers. These commands are directed toward the goal of maintaining blood pressure to the brain and heart, which are treated by the body as the most vital organs. The brain and heart cannot sustain low perfusion for any substantial period of time. A stroke or a cardiac arrest will result if the blood pressure to these organs is reduced to unacceptable levels. Other organs, such as kidneys, can withstand somewhat longer periods of ischemia without suffering long-term damage. Accordingly, the body sacrifices blood supply to these other organs in favor of the brain and the heart.
The hemodynamic impairment resulting from CHF activates several neurohomonal systems, such as the rennin-angiotensin and aldosterone system, sympatho-adrenal system and vasopressin release. As the kidneys suffer from increased renal vasoconstriction, the filtering rate (GFR) of the blood drops and the sodium load in the circulatory system increases. Simultaneously, more renin is liberated from the juxtaglomerular of the kidney 104. The combined effects of reduced kidney functioning include reduced glomerular sodium load, an aldosterone-mediated increase in tubular reabsorption of sodium, and retention in the body of sodium and water. These effects lead to several signs and symptoms of the CHF condition, including an enlarged heart, increased systolic wall stress and an increased myocardial oxygen demand, and the formation of edema on the basis of fluid and sodium retention in the kidney 107. Accordingly, sustained reduction in renal blood flow and vasoconstriction is directly responsible for causing the fluid retention associated with CHF.
Fluid overload is caused in two ways. First, activation of the renin-angiotensin system leads to retention of salt, thus water by the kidney. Second, the persistent lower renal blood flow and pressure cannot generate adequate hydrostatic pressure to make sufficient urine to remove excess retained fluid. Accordingly, the kidneys are a principal non-cardiac cause of a progressive fluid overload condition in a patient suffering from CHF.
C. Prior Treatments for CHF
Many non-surgical therapies are widely used to treat CHF. In general, they include methods of increasing the pumping ability of the heart itself or reducing the work required of the heart to pump blood. These therapies are effective at first but their effects are ultimately exhausted. In addition, no non-surgical therapies have been able to prevent the inexorable decline in circulatory function.
The principal disturbance in CHF is the inability of the heart to perform as a pump leading to a reduced cardiac output. Thus, directly combating the inability of the heart to propel blood forward might seem to be the single most intuitive means for treating heart failure. Utilizing this mechanism, a class of drugs known as inotropes increases the strength of contraction of the heart, allowing the heart to expel more blood with each beat. However, while effective in the short-term, these drugs lack long-term value in the treatment of congestive heart failure.
Patients with CHF can also suffer episodes of acute, severe deterioration caused by abrupt decreases in heart function. These episodes are characterized by rapid reductions in blood pressure and flow, especially to the kidney. Similarly to the chronic state, acutely reduced kidney perfusion can result in a sudden, massive retention of fluid leading to pulmonary edema (fluid in lungs). This acute fluid overload taxes an already overburdened heart and can lead to the severest of complications: acute renal failure and death.
In the intensive care unit, these patients may benefit from short-term use of inotropic therapy (drugs that improve the ability of the heart to squeeze and pump blood) to temporarily improve cardiac output and renal blood flow. Intubation and mechanical ventilation of the lungs are of value in patients with severe hypoxia from fluid overload leading to pulmonary edema. Mechanical ventilation is very effective but is complicated by infections and difficulty in weaning patients off the ventilator. Patients with severe refractory pulmonary edema may also benefit from intra-aortic balloon counterpulsation to assist the heart. However, while very effective in treating refractory angina, intra-aortic balloon pumping has not been shown to have a significant beneficial clinical effect in acute CHF. The inotropic drugs may cause severe arrhythmias (irregular heart beats) that can also lead to death.
Increasing doses of more powerful intravenous diuretics may be used but are increasingly ineffective as the renal perfusion is reduced in response to the maladaptive compensatory response. Over time as heart function further decreases and vasoconstriction further increases, progressively less blood reaches the kidneys, resulting in a progressive inability to excrete fluid and increasingly severe symptoms of fluid overload. Any degree of intrinsic renal insufficiency will also contribute to limiting the effectiveness of diuretic therapy and the patient will continue to retain fluid.
To treat CHF, the physicians must fight the body""s attempt to inflict itself harm. Heart failure patients are put on a strict low sodium diet and their fluid intake is monitored. Some patients are limited to as little as one liter of fluid a day. The most important drugs in the physician""s arsenal to combat fluid overload are the class of drugs called diuretics. Diuretics affect the kidney function in such a way that the reabsorbtion of fluid is suppressed. As a result there is more urine output contrary to neurohormonal commands that the kidney is receiving.
Physicians can treat the patient with agents that improve the pumping ability of the heart, increase blood pressure and attempt to reactivate a more normal behavior of the body""s control (homeostatic) system. In general, this is effective in sustaining life of many heart failure patients. Nevertheless, in hundreds of thousands of patients, treatments with drugs and diet alone fail. The patients are repeatedly admitted to the hospital for intensive care. Ultimately they may require a heart transplant.
When available treatment can no longer achieve adequate fluid removal with existing kidney function, renal replacement therapies such as hemofiltration or dialysis have been increasingly used as a method of removing fluid in the acute CHF state. Acute heart failure can be treated with the Continuous Renal Replacement Therapy (a.k.a, an artificial kidney or dialysis machine) in the ICU of a hospital. The machine is instrumental in reducing fluid overload and preventing such complications as pulmonary edema. At the same time the kidney machine can be harmful to other organs and does not protect the kidney itself from further deterioration from the persistently low blood pressure and poor perfusion caused by vasoconstriction of the renal artery and arterioles (smaller branches). Thus, renal replacement therapy may be used to remove fluid but is associated with significant complications. Its use is limited since it may cause further abrupt reductions in blood pressure, actually worsening the heart failure state and further renal dysfunction. Physicians are reluctant to use it in unstable patients because of added risk of hypotension.
Continuous hemofiltration is a new modality based on a well-established therapy with an artificial kidney (or renal replacement therapy). Blood is continuously extracted from the body, passed through an artificial kidney machine and then returned back to the body. In the process, some of the undesired chemicals can be extracted. Most importantly for acute heart failure patients, fluid can be filtered out of the blood stream in a slow controlled infusion while concentrating the blood.
Blood is a suspension of cells in a fluid called plasma. Plasma contains water and chemicals. The artificial kidney machine allows a physician to control the separation of plasma and adjust the total amount of fluid remaining in the patient""s body. The hemofiltration machine works in parallel with patient""s kidneys and takes over their function.
The artificial kidney does nothing to protect natural kidneys from deterioration and as a result the natural kidneys often suffer progressive damage from hypotension and ischemia. Also, the artificial kidney does not interrupt the renin-angiotensin feedback mechanisms that continue to fight the physician in his or her attempts to save the patient from continued deterioration.
Reversing fluid overload can improve heart function and significantly enhance the clinical status of the CHF patient. Yet, while therapies that improve renal blood flow are beneficial in removing fluid, they are still relatively ineffective. Similarly, while therapies, such as hemofiltration, effectively remove fluid from the patient, they can actually lead to lower blood pressure, further deterioration of the heart and ultimately renal failure requiring the patient to undergo permanent dialysis or kidney transplant.
There is a long-felt need to be able to treat the fluid overload complications of CHF by being able to restore kidney function, without resorting to kidney dialysis. Restoration of kidney function should: (1) return kidney function to normal therefore protecting kidney from hypotension induced damage, (2) remove excess fluid volume from a patient in a safe controlled manner, and/or (3) alter a patient""s neurohormonal environment. Such CHF treatment should decrease or eliminate the physical signs and symptoms of congestive heart failure, improving both a patient""s quality of life and survival rate. The present invention provides a method to reduce the morbidity and mortality associated with congestive heart failure in patients by restoration of renal perfusion pressure.
The invention is a novel method and apparatus of treating acute and chronic CHF by restoration of renal perfusion pressure. Restoration of acceptable blood pressure applied directly applied to one or both kidneys of a patient with heart failure significantly improves renal blood flow, removes excess body fluids and improve the patient""s overall condition. In addition, restoring renal perfusion pressure to the kidney suppresses, the deleterious activation of the renin-angiotensin system and the consequences of its widespread adverse effects on CHF patients as is shown in FIG. 7. Increased fluid removal results from the restoration of a hydrostatic gradient 110 across the kidney by increasing renal blood flow under increased renal perfusion pressure. The level of effectiveness of this method is substantially above the levels achieved by drug therapy.
Restoring renal perfusion 111, should result in increased urine output 112 and a decrease in the neurohormaonal stimulation 113 caused by kidneys in a failing condition. This decrease in stimulation by the kidneys is expected to decrease the vasoconstriction 114 in the patient""s circulatory system, and decrease the amount of sodium and fluid retention 115 in the patient. In turn, increased urine output, reduced vasoconstriction, and decreased sodium level should restore normal fluid balances in the patient, improve oxygenation of the blood and decrease the heart workload 116. Heart function should improve 117 due to the reduction in its workload and the other beneficial effects due to renal perfusion. Moreover, a stronger heart and higher blood pressure will improve the perfusion of other organs 118 and thereby normalize the acid-base metabolism 119 to further improve the workload, etc. on the heart.
The system for treating CHF disclosed here restores kidney functioning and thereby breaks the cycle between heart and kidney failure. This type of CHF treatment is new, novel and unobvious. Moreover, this treatment may be used in connection with other CHF treatments that directly treat the heart, and may be used for both chronic and acute CHF.
For treating acute CHF, an invasive catheter system has been developed by applicants to perfuse the kidneys. This catheter system is described more fully in the co-owned and related U.S. application Ser. No. 09/454,605 for a xe2x80x9cKidney Perfusion Catheterxe2x80x9d, identified above. The catheter is inserted at the patient""s groin and into the femoral artery. The catheter maneuvered by a surgeon through the femoral artery, into the aorta to the entrance of one of the renal arteries. Blood enters a proximal end of the catheter from a blood pump and flows from the distal end of the catheter directly into the renal artery. This blood flow perfuses the kidney and rapidly restores adequate kidney functions to one kidney.
Apparatuses for treating chronic CHF may include an implantable device, e.g., using a prosthesis vein or artery, having a distal end coupled to one of the renal arteries and a proximal end coupled to a fluid port implanted under the patient""s skin. Kidneys reside deep in the body and cannot be reached easily from the body surface with a needle or a catheter. To perfuse the kidney, a conduit to a blood pump is attached to the patient""s fluid port coupling to cause blood to flow from the pump through the implanted device to the renal artery. The patient is connected to the blood pump periodically to perfuse the kidney, without having to surgically insert a catheter into the patient.
Alternatively, a blood pump and passageway between a vein and a renal artery may be implanted in a patient. The blood pump controls a flow of blood from the vein, through the passageway, and into the renal artery to perfuse the kidney. The blood pump may be remotely controlled by the patient or doctor to operate periodically to perfuse the kidney. More detailed descriptions of implantable devices are disclosed in the commonly-owned PCT Application No. WO 01/97879 entitled xe2x80x9cApparatus And Method for Perfusing The Kidney With Venous Bloodxe2x80x9d; PCT Application No. WO 01/97717 entitled xe2x80x9cImplantable Flow Diversion Devicexe2x80x9d; PCT Application No. WO 01/97878 entitled xe2x80x9cSplit Circulation Devicexe2x80x9d; PCT Application No. WO 01/97717 entitled xe2x80x9cInstrumented Stentxe2x80x9d; U.S. Pat. No. 6,241,743 entitled xe2x80x9cAnastomosis Device And Methodxe2x80x9d.